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[PMID]:28743992
[Au] Autor:Cao J; Peng J; An H; He Q; Boronina T; Guo S; White MF; Cole PA; He L
[Ad] Endereço:Division of Metabolism, Department of Pediatrics, Johns Hopkins University School of Medicine, Baltimore, MD, 21287, USA.
[Ti] Título:Endotoxemia-mediated activation of acetyltransferase P300 impairs insulin signaling in obesity.
[So] Source:Nat Commun;8(1):131, 2017 07 25.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Diabetes and obesity are characterized by insulin resistance and chronic low-grade inflammation. An elevated plasma concentration of lipopolysaccharide (LPS) caused by increased intestinal permeability during diet-induced obesity promotes insulin resistance in mice. Here, we show that LPS induces endoplasmic reticulum (ER) stress and protein levels of P300, an acetyltransferase involved in glucose production. In high-fat diet fed and genetically obese ob/ob mice, P300 translocates from the nucleus into the cytoplasm of hepatocytes. We also demonstrate that LPS activates the transcription factor XBP1 via the ER stress sensor IRE1, resulting in the induction of P300 which, in turn, acetylates IRS1/2, inhibits its association with the insulin receptor, and disrupts insulin signaling. Pharmacological inhibition of P300 acetyltransferase activity by a specific inhibitor improves insulin sensitivity and decreases hyperglycemia in obese mice. We suggest that P300 acetyltransferase activity may be a promising therapeutic target for the treatment of obese patients.Elevated plasma LPS levels have been associated with insulin resistance. Here Cao et al. show that LPS induces ER stress and P300 activity via the XBP1/IRE1 pathway. P300 acetylates IRS1/2 and inhibits its binding with the insulin receptor. The consequent impairment of insulin signaling can be rescued by pharmacological inhibition of P300.
[Mh] Termos MeSH primário: Proteína p300 Associada a E1A/metabolismo
Endotoxemia/metabolismo
Insulina/metabolismo
Obesidade/metabolismo
Transdução de Sinais
[Mh] Termos MeSH secundário: Animais
Linhagem Celular Tumoral
Proteína p300 Associada a E1A/genética
Estresse do Retículo Endoplasmático/efeitos dos fármacos
Estresse do Retículo Endoplasmático/genética
Perfilação da Expressão Gênica/métodos
Immunoblotting
Resistência à Insulina
Lipopolissacarídeos/farmacologia
Fígado/efeitos dos fármacos
Fígado/metabolismo
Masculino
Proteínas de Membrana/genética
Proteínas de Membrana/metabolismo
Camundongos Endogâmicos C57BL
Camundongos Obesos
Obesidade/genética
Proteínas Serina-Treonina Quinases/genética
Proteínas Serina-Treonina Quinases/metabolismo
Receptor de Insulina/genética
Receptor de Insulina/metabolismo
Proteína 1 de Ligação a X-Box/genética
Proteína 1 de Ligação a X-Box/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Insulin); 0 (Lipopolysaccharides); 0 (Membrane Proteins); 0 (X-Box Binding Protein 1); 0 (Xbp1 protein, mouse); EC 2.3.1.48 (E1A-Associated p300 Protein); EC 2.7.1.- (Ern2 protein, mouse); EC 2.7.10.1 (Receptor, Insulin); EC 2.7.11.1 (Protein-Serine-Threonine Kinases)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:180217
[Lr] Data última revisão:
180217
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170727
[St] Status:MEDLINE
[do] DOI:10.1038/s41467-017-00163-w


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[PMID]:29179781
[Au] Autor:Pei R; DiMarco DM; Putt KK; Martin DA; Gu Q; Chitchumroonchokchai C; White HM; Scarlett CO; Bruno RS; Bolling BW
[Ad] Endereço:1Department of Nutritional Sciences,University of Connecticut,3624 Horsebarn Road Extension,Unit 4017,Storrs,CT 06269,USA.
[Ti] Título:Low-fat yogurt consumption reduces biomarkers of chronic inflammation and inhibits markers of endotoxin exposure in healthy premenopausal women: a randomised controlled trial.
[So] Source:Br J Nutr;118(12):1043-1051, 2017 Dec.
[Is] ISSN:1475-2662
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The anti-inflammatory mechanisms of low-fat dairy product consumption are largely unknown. The objective of this study was to determine whether low-fat yogurt reduces biomarkers of chronic inflammation and endotoxin exposure in women. Premenopausal women (BMI 18·5-27 and 30-40 kg/m2) were randomised to consume 339 g of low-fat yogurt (yogurt non-obese (YN); yogurt obese (YO)) or 324 g of soya pudding (control non-obese; control obese (CO)) daily for 9 weeks (n 30/group). Fasting blood samples were analysed for IL-6, TNF-α/soluble TNF II (sTNF-RII), high-sensitivity C-reactive protein, 2-arachidonoyl glycerol, anandamide, monocyte gene expression, soluble CD14 (sCD14), lipopolysaccharide (LPS), LPS binding protein (LBP), IgM endotoxin-core antibody (IgM EndoCAb), and zonulin. BMI, waist circumference and blood pressure were also determined. After 9-week yogurt consumption, YO and YN had decreased TNF-α/sTNFR-RII. Yogurt consumption increased plasma IgM EndoCAb regardless of obesity status. sCD14 was not affected by diet, but LBP/sCD14 was lowered by yogurt consumption in both YN and YO. Yogurt intervention increased plasma 2-arachidonoylglycerol in YO but not YN. YO peripheral blood mononuclear cells expression of NF-κB inhibitor α and transforming growth factor ß1 increased relative to CO at 9 weeks. Other biomarkers were unchanged by diet. CO and YO gained approximately 0·9 kg in body weight. YO had 3·6 % lower diastolic blood pressure at week 3. Low-fat yogurt for 9 weeks reduced biomarkers of chronic inflammation and endotoxin exposure in premenopausal women compared with a non-dairy control food. This trial was registered as NCT01686204.
[Mh] Termos MeSH primário: Biomarcadores/sangue
Dieta
Endotoxinas/toxicidade
Inflamação/sangue
Inflamação/dietoterapia
Iogurte/análise
[Mh] Termos MeSH secundário: Proteínas da Fase Aguda
Adulto
Antropometria
Ácidos Araquidônicos/sangue
Proteína C-Reativa/metabolismo
Proteínas de Transporte/sangue
Doença Crônica
Citocinas/sangue
Gorduras na Dieta/administração & dosagem
Gorduras na Dieta/análise
Endocanabinoides/sangue
Endotoxemia/sangue
Endotoxemia/dietoterapia
Feminino
Glicerídeos/sangue
Seres Humanos
Imunoglobulina M/sangue
Leucócitos Mononucleares/metabolismo
Glicoproteínas de Membrana/sangue
Meia-Idade
NF-kappa B/metabolismo
Obesidade/metabolismo
Alcamidas Poli-Insaturadas/sangue
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
0 (Acute-Phase Proteins); 0 (Arachidonic Acids); 0 (Biomarkers); 0 (Carrier Proteins); 0 (Cytokines); 0 (Dietary Fats); 0 (Endocannabinoids); 0 (Endotoxins); 0 (Glycerides); 0 (Immunoglobulin M); 0 (Membrane Glycoproteins); 0 (NF-kappa B); 0 (Polyunsaturated Alkamides); 0 (lipopolysaccharide-binding protein); 8D239QDW64 (glyceryl 2-arachidonate); 9007-41-4 (C-Reactive Protein); UR5G69TJKH (anandamide)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180207
[Lr] Data última revisão:
180207
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171129
[Cl] Clinical Trial:ClinicalTrial
[St] Status:MEDLINE
[do] DOI:10.1017/S0007114517003038


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[PMID]:29215240
[Au] Autor:Poryadin GV; Vlasov AP; Trofimov VA; Vlasova TI; Kamkina OV; Grigoryev AG; Vlasov PA
[Ti] Título:[Hemoglobin oxygen transport capacity in surgical endotoxicosis ].
[So] Source:Patol Fiziol Eksp Ter;60(1):23-7, 2016 Jan-Mar.
[Is] ISSN:0031-2991
[Cp] País de publicação:Russia (Federation)
[La] Idioma:rus
[Ab] Resumo:In surgical endointoxication hemoglobin oxygen transport capacity of red blood cells (hemoglobin affinity ligands: the ability to bind and release ligands) is reduced and is associated with the severity of endogenous intoxication. Violation of oxygen transport function of hemoglobin at endogenous intoxication is associated with conformational changes of a biomolecule, and its possible influence on reactive oxygen species, which confirmed in experiments in vitro: under the influence of oxygen-iron ascorbate ability of hemoglobin deteriorates. Largely similar structural and functional changes in hemoglobin occur in patients with surgical endotoxicosis.
[Mh] Termos MeSH primário: Endotoxemia/metabolismo
Eritrócitos/metabolismo
Hemoglobinas/metabolismo
Oxigênio/metabolismo
Complicações Pós-Operatórias/metabolismo
[Mh] Termos MeSH secundário: Adulto
Transporte Biológico Ativo
Endotoxemia/etiologia
Eritrócitos/patologia
Feminino
Seres Humanos
Masculino
Meia-Idade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Hemoglobins); S88TT14065 (Oxygen)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171221
[Lr] Data última revisão:
171221
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171208
[St] Status:MEDLINE


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[PMID]:28464257
[Au] Autor:Pang J; Xu W; Zhang X; Wong GL; Chan AW; Chan HY; Tse CH; Shu SS; Choi PC; Chan HL; Yu J; Wong VW
[Ad] Endereço:Department of Medicine and Therapeutics, The Chinese University of Hong Kong, Shatin, Hong Kong.
[Ti] Título:Significant positive association of endotoxemia with histological severity in 237 patients with non-alcoholic fatty liver disease.
[So] Source:Aliment Pharmacol Ther;46(2):175-182, 2017 07.
[Is] ISSN:1365-2036
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Patients with nonalcoholic steatohepatitis (NASH) have gut dysbiosis and intestinal bacterial overgrowth. AIM: To test the hypothesis that endotoxemia is associated with the histological severity of nonalcoholic fatty liver disease (NAFLD) and determine factors associated with endotoxemia. METHODS: The endotoxemia markers lipopolysaccharide-binding protein (LBP) and endotoxin levels were measured in 237 NAFLD patients 1 day before liver biopsy. Biomarkers of liver injury and transient elastography were performed as additional markers of disease severity. RESULTS: A total of 114/237 (48%) patients had NASH and 80/237 (34%) had F2-4 fibrosis. LBP was correlated with lobular inflammation (P=.001), while both LBP (P=.0004) and endotoxin levels (P=0.008) were correlated with fibrosis. LBP was also correlated with cytokeratin-18 fragments (P=.002) and aspartate aminotransferase-to-alanine aminotransferase ratio (P=.006), and both LBP (P=.019) and endotoxin (P=.006) were correlated with liver stiffness measurement by transient elastography. LBP was increased in patients with NASH (15.3±4.6 vs 13.8±3.3 µg/mL; P=.005) and F2-4 fibrosis (15.4±4.4 vs 14.0±3.7 µg/mL; P=.008). Interestingly, patients harbouring the TM6SF2 rs58542926 T allele that predispose to NAFLD/NASH had higher LBP level. By multivariate analysis, gender, higher body mass index and glycated haemoglobin, and TM6SF2 variants were independent factors associated with increased LBP level. CONCLUSIONS: Endotoxemia is positively associated with NASH and significant fibrosis. The association between TM6SF2 and endotoxemia warrants further investigations. The findings may shed light on the pathogenesis of NASH and inform a novel treatment target.
[Mh] Termos MeSH primário: Endotoxemia/epidemiologia
Hepatopatia Gordurosa não Alcoólica/epidemiologia
[Mh] Termos MeSH secundário: Proteínas da Fase Aguda
Adulto
Idoso
Alelos
Biomarcadores
Biópsia
Índice de Massa Corporal
Proteínas de Transporte/sangue
Feminino
Fibrose
Seres Humanos
Intestinos/microbiologia
Queratina-18/sangue
Fígado/patologia
Masculino
Glicoproteínas de Membrana/sangue
Meia-Idade
Índice de Gravidade de Doença
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Acute-Phase Proteins); 0 (Biomarkers); 0 (Carrier Proteins); 0 (Keratin-18); 0 (Membrane Glycoproteins); 0 (lipopolysaccharide-binding protein)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171220
[Lr] Data última revisão:
171220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE
[do] DOI:10.1111/apt.14119


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[PMID]:28470577
[Au] Autor:Bannert E; Tesch T; Kluess J; Valenta H; Frahm J; Kersten S; Kahlert S; Renner L; Rothkötter HJ; Dänicke S
[Ad] Endereço:Institute of Animal Nutrition, Friedrich-Loeffler-Institute (FLI), Federal Research Institute for Animal Health, Bundesallee 50, 38116, Braunschweig, Germany.
[Ti] Título:Plasma kinetics and matrix residues of deoxynivalenol (DON) and zearalenone (ZEN) are altered in endotoxaemic pigs independent of LPS entry site.
[So] Source:Mycotoxin Res;33(3):183-195, 2017 Aug.
[Is] ISSN:1867-1632
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:This study aimed to investigate a potential modulatory effect of E. coli lipopolysaccharide (LPS) on the kinetics of deoxynivalenol (DON) and zearalenone (ZEN) after pre- or post-hepatic LPS administration to unravel the putative role of the liver. Fifteen barrows were fed a diet containing mycotoxin-contaminated maize (4.59 mg DON/kg feed, 0.22 mg ZEN/kg feed) for 29 days and equipped with pre-hepatic catheters (portal vein, "po") and post-hepatic catheters (jugular vein, "ju"), facilitating simultaneous infusion of LPS ("LPS group", 7.5 µg/kg body weight) or 0.9% sterile NaCl solution (control, "CON group", equivolumar to LPS group) and blood sampling. This resulted in three infusion groups, depending on infusion site: CON -CON , CON -LPS , and LPS -CON . On day 29, pigs were fed their morning ration (700 g/pig) (-15 min), and blood samples were collected at regular intervals relative to infusion start. At 195 min, pigs were sacrificed and bile, urine, liquor, and liver samples collected. DON concentrations in jugular and portal blood decreased in both LPS-infused groups, whereas the ZEN concentrations increased, regardless of the treatment site. In liver tissue, a decrease of both toxin concentrations was observed in endotoxaemic pigs as well as a drop in hepatic conjugation, regardless of LPS entry site. In contrast to our hypothesis, DON and ZEN were not differently altered depending on the LPS-entry site. Neither the absorption nor the accumulation of DON and ZEN in different tissues differed significantly between animals which were infused with LPS via either the jugular or portal vein.
[Mh] Termos MeSH primário: Endotoxemia/sangue
Lipopolissacarídeos/administração & dosagem
Suínos/sangue
Tricotecenos/sangue
Zearalenona/sangue
[Mh] Termos MeSH secundário: Ração Animal
Animais
Escherichia coli
Contaminação de Alimentos
Cinética
Tricotecenos/farmacocinética
Zearalenona/farmacocinética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Lipopolysaccharides); 0 (Trichothecenes); 5W827M159J (Zearalenone); JT37HYP23V (deoxynivalenol)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171218
[Lr] Data última revisão:
171218
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE
[do] DOI:10.1007/s12550-017-0276-z


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[PMID]:28848068
[Au] Autor:Vandereyken MM; Singh P; Wathieu CP; Jacques S; Zurashvilli T; Dejager L; Amand M; Musumeci L; Singh M; Moutschen MP; Libert CRF; Rahmouni S
[Ad] Endereço:Immunology and Infectious Disease Unit, GIGA-Research, University of Liège, B-4000 Liège, Belgium.
[Ti] Título:Dual-Specificity Phosphatase 3 Deletion Protects Female, but Not Male, Mice from Endotoxemia-Induced and Polymicrobial-Induced Septic Shock.
[So] Source:J Immunol;199(7):2515-2527, 2017 Oct 01.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Dual-specificity phosphatase 3 (DUSP3) is a small phosphatase with poorly known physiological functions and for which only a few substrates are known. Using knockout mice, we recently reported that DUSP3 deficiency confers resistance to endotoxin- and polymicrobial-induced septic shock. We showed that this protection was macrophage dependent. In this study, we further investigated the role of DUSP3 in sepsis tolerance and showed that the resistance is sex dependent. Using adoptive-transfer experiments and ovariectomized mice, we highlighted the role of female sex hormones in the phenotype. Indeed, in ovariectomized females and in male mice, the dominance of M2-like macrophages observed in DUSP3 female mice was reduced, suggesting a role for this cell subset in sepsis tolerance. At the molecular level, DUSP3 deletion was associated with estrogen-dependent decreased phosphorylation of ERK1/2 and Akt in peritoneal macrophages stimulated ex vivo by LPS. Our results demonstrate that estrogens may modulate M2-like responses during endotoxemia in a DUSP3-dependent manner.
[Mh] Termos MeSH primário: Fosfatases de Especificidade Dupla/genética
Fosfatases de Especificidade Dupla/metabolismo
Endotoxemia/enzimologia
Endotoxemia/prevenção & controle
Estrogênios/metabolismo
Macrófagos/fisiologia
Choque Séptico/prevenção & controle
[Mh] Termos MeSH secundário: Animais
Coinfecção/complicações
Fosfatases de Especificidade Dupla/deficiência
Endotoxemia/genética
Endotoxemia/microbiologia
Feminino
Tolerância Imunológica
Lipopolissacarídeos/imunologia
Sistema de Sinalização das MAP Quinases/efeitos dos fármacos
Macrófagos/efeitos dos fármacos
Macrófagos/imunologia
Masculino
Camundongos
Camundongos Knockout
Ovariectomia
Fosforilação
Caracteres Sexuais
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Estrogens); 0 (Lipopolysaccharides); EC 3.1.3.48 (Dual-Specificity Phosphatases)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171024
[Lr] Data última revisão:
171024
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170830
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1602092


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[PMID]:28842383
[Au] Autor:Arana MR; Tocchetti GN; Zecchinati F; Londero AS; Dominguez C; Perdomo V; Rigalli JP; Villanueva SSM; Mottino AD
[Ad] Endereço:Instituto de Fisiología Experimental (CONICET), Facultad de Ciencias Bioquímicas y Farmacéuticas (UNR), Suipacha 570, 2000, Rosario, Argentina.
[Ti] Título:Glucagon-like peptide 2 prevents down-regulation of intestinal multidrug resistance-associated protein 2 and P-glycoprotein in endotoxemic rats.
[So] Source:Toxicology;390:22-31, 2017 Sep 01.
[Is] ISSN:1879-3185
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:Multidrug resistance-associated protein 2 (Mrp2, ABCC2) and P-glycoprotein (P-gp, ABCB1) constitute essential components of the intestinal biochemical barrier that prevent incorporation of food contaminants, drugs or toxic metabolites into the blood stream. Endotoxemia induced in rats by administration of bacterial lipopolysaccharide (LPS) results in elevated intestinal permeability and toxicity of xenobiotics in part associated with down-regulation of expression and activity of Mrp2 and P-gp. We evaluated the protective effect of glucagon-like peptide 2 (GLP-2), a peptide hormone with enterotrophic properties, on Mrp2 and P-gp alterations induced by single i.p. injection of LPS (5mg/kg b.wt.) to rats. Two different protocols of GLP-2 administration, namely prevention and reversion, were examined. The prevention protocol consisted of 7s.c. injections of GLP-2 (125µg/kg b.wt.) administered every 12h, starting 60h before LPS administration. The reversion protocol consisted of 2 doses of GLP-2, starting 3h after LPS injection. Intestinal samples were collected 24h after LPS administration and expression (protein and mRNA) and activity of Mrp2 were evaluated in proximal jejunum whereas those of P-gp were studied in ileum. GLP-2 completely neutralized down-regulation of expression of Mrp2 and P-gp and loss of their respective activities induced by LPS under prevention protocol. GLP-2 was also able to prevent internalization of both transporters from the apical membrane of the enterocyte to intracellular compartments, as detected by confocal microscopy. LPS induced an increase in IL-1ß and oxidized glutathione tissue levels, which were also counterbalanced by GLP-2 administration. In contrast, the reversion protocol failed to attenuate Mrp2 and P-gp down-regulation induced by LPS. We conclude that GLP-2 can prevent down-regulation of intestinal expression and activity of Mrp2 and P-gp in endotoxemic rats and that IL-1ß and oxidative stress constitute potential targets of GLP-2 protective effects.
[Mh] Termos MeSH primário: Transportadores de Cassetes de Ligação de ATP/metabolismo
Endotoxemia/prevenção & controle
Peptídeo 2 Semelhante ao Glucagon/administração & dosagem
Jejuno/metabolismo
[Mh] Termos MeSH secundário: Subfamília B de Transportador de Cassetes de Ligação de ATP/genética
Subfamília B de Transportador de Cassetes de Ligação de ATP/metabolismo
Transportadores de Cassetes de Ligação de ATP/genética
Animais
Antioxidantes/metabolismo
Modelos Animais de Doenças
Regulação para Baixo
Esquema de Medicação
Endotoxemia/induzido quimicamente
Endotoxemia/metabolismo
Feminino
Glutationa/metabolismo
Injeções Subcutâneas
Interleucina-1beta/metabolismo
Absorção Intestinal
Lipopolissacarídeos
Oxirredução
Estresse Oxidativo/efeitos dos fármacos
Permeabilidade
Ratos Wistar
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ATP Binding Cassette Transporter, Sub-Family B); 0 (Abcc2 protein, rat); 0 (Antioxidants); 0 (Glucagon-Like Peptide 2); 0 (IL1B protein, rat); 0 (Interleukin-1beta); 0 (Lipopolysaccharides); 0 (multidrug resistance protein 3); GAN16C9B8O (Glutathione)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170827
[St] Status:MEDLINE


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[PMID]:28815345
[Au] Autor:Xu H; Xiong J; Xu J; Li S; Zhou Y; Chen D; Cai X; Ping J; Deng M; Chen J
[Ad] Endereço:Department of Gastroenterology and Hepatology, Hangzhou Red Cross Hospital, 208 Huancheng Dong Road, Hangzhou, 310003, China.
[Ti] Título:Mosapride Stabilizes Intestinal Microbiota to Reduce Bacterial Translocation and Endotoxemia in CCl -Induced Cirrhotic Rats.
[So] Source:Dig Dis Sci;62(10):2801-2811, 2017 Oct.
[Is] ISSN:1573-2568
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Impaired intestinal motility may lead to the disruption of gut microbiota equilibrium, which in turn facilitates bacterial translocation (BT) and endotoxemia in cirrhosis. We evaluated the influence of mosapride, a prokinetic agent, on BT and DNA fingerprints of gut microbiota in cirrhotic rats. METHODS: A rat model of cirrhosis was set up via subcutaneous injection of carbon tetrachloride (CCl ). The portal pressure, liver and intestinal damage, plasma endotoxin, BT, and intestinal transit rate (ITR) of cirrhotic rats were determined. Fecal DNA fingerprints were obtained by ERIC-PCR. The expressions of tight junction proteins were evaluated by western blotting. RESULTS: Mosapride treatment to cirrhotic rats significantly reduced the plasma endotoxin level and incidence of BT, accompanied by increased ITR. Cirrhotic rats (including those treated with mosapride) suffered from BT exhibited significantly lower ITR than those who are free of BT. Pearson coefficient indicated a significant and negative correlation between the plasma endotoxin level and ITR. The genomic fingerprints of intestinal microbiota from the three groups fell into three distinctive clusters. In the mosapride-treated group, Shannon's index was remarkably increased compared to the model group. Significantly positive correlation was detected between Shannon's index and ITR. Mosapride did not improve hepatic and intestinal damages and ileal expressions of occludin and ZO-1. CONCLUSIONS: Mosapride significantly increases intestinal motility in cirrhotic rats, thus to recover the disordered intestinal microbiota, finally resulting in decreased plasma endotoxin and BT.
[Mh] Termos MeSH primário: Translocação Bacteriana/efeitos dos fármacos
Benzamidas/farmacologia
Tetracloreto de Carbono
Doença Hepática Induzida por Substâncias e Drogas/prevenção & controle
Endotoxemia/prevenção & controle
Fármacos Gastrointestinais/farmacologia
Microbioma Gastrointestinal/efeitos dos fármacos
Intestinos/efeitos dos fármacos
Cirrose Hepática Experimental/prevenção & controle
Fígado/efeitos dos fármacos
Morfolinas/farmacologia
[Mh] Termos MeSH secundário: Animais
Doença Hepática Induzida por Substâncias e Drogas/sangue
Doença Hepática Induzida por Substâncias e Drogas/microbiologia
Doença Hepática Induzida por Substâncias e Drogas/patologia
DNA Bacteriano/genética
Endotoxemia/sangue
Endotoxemia/induzido quimicamente
Endotoxemia/microbiologia
Endotoxemia/patologia
Fezes/microbiologia
Motilidade Gastrointestinal/efeitos dos fármacos
Intestinos/metabolismo
Intestinos/microbiologia
Intestinos/patologia
Fígado/metabolismo
Fígado/microbiologia
Fígado/patologia
Cirrose Hepática Experimental/sangue
Cirrose Hepática Experimental/microbiologia
Cirrose Hepática Experimental/patologia
Masculino
Ratos Sprague-Dawley
Proteínas de Junções Íntimas/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Benzamides); 0 (DNA, Bacterial); 0 (Gastrointestinal Agents); 0 (Morpholines); 0 (Tight Junction Proteins); CL2T97X0V0 (Carbon Tetrachloride); I8MFJ1C0BY (mosapride)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171024
[Lr] Data última revisão:
171024
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170818
[St] Status:MEDLINE
[do] DOI:10.1007/s10620-017-4704-x


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[PMID]:28807827
[Au] Autor:Zhang J; Zhao P; Quan N; Wang L; Chen X; Cates C; Rousselle T; Li J
[Ad] Endereço:Department of Nutrition, Shandong Provincial Hospital Affiliated to Shandong University, Jinan, China; Department of Physiology and Biophysics, Mississippi Center for Heart Research, University of Mississippi Medical Center, Jackson, MS, USA.
[Ti] Título:The endotoxemia cardiac dysfunction is attenuated by AMPK/mTOR signaling pathway regulating autophagy.
[So] Source:Biochem Biophys Res Commun;492(3):520-527, 2017 Oct 21.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:AMP-activated protein kinase (AMPK), an enzyme that plays a role in cellular energy homeostasis, modulates myocardial signaling in the heart. Myocardial dysfunction is a common complication of sepsis. Autophagy is involved in the aging related cardiac dysfunction. However, the role of AMPK in sepsis-induced cardiotoxicity has yet to be clarified, especially in aging. In this study, we explored the role of AMPK in lipopolysaccharide (LPS)-induced myocardial dysfunction and elucidated the potential mechanisms of AMPK/mTOR pathway regulating autophagy in young and aged mice. We harvested cardiac tissues by intraperitoneal injection of LPS treatment. The results by echocardiography, pathology, contractile and intracellular Ca property as well as western blot analysis revealed that LPS induced remarkable cardiac dysfunction and cardiotoxicity in mice hearts and cardiomyocytes, which were more seriously in the aged mice. Western blot analysis indicated that the underlying mechanisms included inhibition autophagy mediated by AMPK/mTOR activation. LPS overtly promoted the expression of AMPK upstream regulator PP2A and PP2Cα. Pharmacological activation of AMPK improved cardiac function and upregulated cardiac autophagy induced by LPS in the aged mice. Collectively, our findings suggest that upregulation of autophagy by administration of AMPK could attenuate LPS-induced cardiotoxicity, which enhances our knowledge to explore new drugs and strategies for combating cardiac dysfunction induced by sepsis.
[Mh] Termos MeSH primário: Proteínas Quinases Ativadas por AMP/metabolismo
Autofagia
Endotoxemia/metabolismo
Miocárdio/metabolismo
Transdução de Sinais
Serina-Treonina Quinases TOR/metabolismo
[Mh] Termos MeSH secundário: Animais
Ecocardiografia
Masculino
Camundongos
Camundongos Endogâmicos C57BL
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
EC 2.7.1.1 (TOR Serine-Threonine Kinases); EC 2.7.1.1 (mTOR protein, mouse); EC 2.7.11.31 (AMP-Activated Protein Kinases)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170816
[St] Status:MEDLINE


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[PMID]:28793772
[Au] Autor:López-Moreno J; García-Carpintero S; Jimenez-Lucena R; Haro C; Rangel-Zúñiga OA; Blanco-Rojo R; Yubero-Serrano EM; Tinahones FJ; Delgado-Lista J; Pérez-Martínez P; Roche HM; López-Miranda J; Camargo A
[Ad] Endereço:Lipids and Atherosclerosis Research Unit, Maimonides Biomedical Research Institute of Cordoba (IMIBIC), Reina Sofia University Hospital, University of Cordoba , 14004 Cordoba, Spain.
[Ti] Título:Effect of Dietary Lipids on Endotoxemia Influences Postprandial Inflammatory Response.
[So] Source:J Agric Food Chem;65(35):7756-7763, 2017 Sep 06.
[Is] ISSN:1520-5118
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Metabolic syndrome (MetS) results in postprandial metabolic alterations that predisposes one to a state of chronic low-grade inflammation and increased oxidative stress. We aimed to assess the effect of the consumption of the quantity and quality of dietary fat on fasting and postprandial plasma lipopolysaccharides (LPS). A subgroup of 75 subjects with metabolic syndrome was randomized to receive 1 of 4 diets: HSFA, rich in saturated fat; HMUFA, rich in monounsaturated fat; LFHCC n-3, low-fat, rich in complex carbohydrate diet supplemented with n-3 polyunsaturated fatty acids; LFHCC low-fat, rich in complex carbohydrate diet supplemented with placebo, for 12 weeks each. We administered a fat challenge reflecting the fatty acid composition of the diets at postintervention. We determined the plasma lipoproteins and glucose and gene expression in peripheral blood mononuclear cells (PBMC) and adipose tissue. LPS and LPS binding protein (LBP) plasma levels were determined by ELISA, at fasting and postprandial (4 h after a fat challenge) states. We observed a postprandial increase in LPS levels after the intake of the HSFA meal, whereas we did not find any postprandial changes after the intake of the other three diets. Moreover, we found a positive relationship between the LPS plasma levels and the gene expression of IkBa and MIF1 in PBMC. No statistically significant differences in the LBP plasma levels at fasting or postprandial states were observed. Our results suggest that the consumption of HSFA diet increases the intestinal absorption of LPS which, in turn, increases postprandial endotoxemia levels and the postprandial inflammatory response.
[Mh] Termos MeSH primário: Gorduras na Dieta/metabolismo
Endotoxemia/dietoterapia
Síndrome Metabólica/dietoterapia
Período Pós-Prandial/imunologia
[Mh] Termos MeSH secundário: Gorduras na Dieta/análise
Endotoxemia/imunologia
Endotoxemia/metabolismo
Feminino
Seres Humanos
Leucócitos Mononucleares/imunologia
Hormônio Inibidor da Liberação de MSH/genética
Hormônio Inibidor da Liberação de MSH/imunologia
Masculino
Síndrome Metabólica/imunologia
Síndrome Metabólica/metabolismo
Meia-Idade
Estresse Oxidativo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
0 (Dietary Fats); 9083-38-9 (MSH Release-Inhibiting Hormone)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170811
[St] Status:MEDLINE
[do] DOI:10.1021/acs.jafc.7b01909



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